Potent inhibition of gastric acid secretion by intravenous interleukin-1 beta and -1 alpha in rats

Peptides. 1992 Mar-Apr;13(2):221-6. doi: 10.1016/0196-9781(92)90100-h.


The influence of human and rat recombinant interleukin-1 (hIL-1 beta and -1 alpha and rIL-1 beta) on acid secretion was investigated in conscious pylorus-ligated rats. Intravenous injection of either hIL-1 beta, hIL-1 alpha or rIL-1 beta dose dependently inhibited gastric acid output with an ED50 of 0.05 microgram, 0.5 microgram and 2.2 micrograms, respectively. The antisecretory action of IL-1 beta was associated with an increase in circulating levels of gastrin. hIL-1 beta-induced inhibition of acid secretion was dose dependently reversed by peripheral injection of the IL-1 receptor antagonist, IL-RA, with a dose ratio of 1:10(3) for complete reversal. The inhibitory effect of hIL-1 beta was blocked by indomethacin and was not modified by IV injections of the CRF receptor antagonist, alpha-helical CRF(9-41), or the monoclonal somatostatin antibody CURE.S6, or by systemic capsaicin pretreatment. These results show that systemic hIL-1 beta-induced inhibition of gastric acid secretion is mediated through IL-1 receptors and prostaglandin pathways, and does not involves CRF receptors, afferent fibers, or changes in circulating gastrin or somatostatin levels.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Corticotropin-Releasing Hormone / antagonists & inhibitors
  • Gastric Acid / metabolism*
  • Humans
  • Indomethacin / pharmacology
  • Injections, Intravenous
  • Interleukin-1 / administration & dosage
  • Interleukin-1 / pharmacology*
  • Male
  • Parietal Cells, Gastric / drug effects*
  • Parietal Cells, Gastric / metabolism
  • Rats
  • Rats, Inbred Strains
  • Recombinant Proteins / administration & dosage
  • Recombinant Proteins / pharmacology


  • Interleukin-1
  • Recombinant Proteins
  • Corticotropin-Releasing Hormone
  • Indomethacin